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吗啡抑制神经修复及吗啡诱导神经损伤的病理学机制是通过内质网应激介导的。

The Pathology of Morphine-Inhibited Nerve Repair and Morphine-Induced Nerve Damage Is Mediated via Endoplasmic Reticulum Stress.

作者信息

Liu Jie, Yi Shanyong, Shi Weibo, Zhang Guozhong, Wang Songjun, Qi Qian, Cong Bin, Li Yingmin

机构信息

Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, China.

Research Center of Basic Medical Sciences, Department of Pathology, School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, China.

出版信息

Front Neurosci. 2021 Feb 19;15:618190. doi: 10.3389/fnins.2021.618190. eCollection 2021.

DOI:10.3389/fnins.2021.618190
PMID:33679302
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7935558/
Abstract

OBJECTIVE

The aim of the present study was to observe the pathological damage in the cerebral cortex of rats under acute morphine exposure (AME) and different durations of morphine dependence (MD), explore whether endoplasmic reticulum stress (ERS) is involved in the damage process, and assess the effect of morphine exposure on the proliferation and differentiation of newborn neurons.

METHODS

Rat models of AME and different durations of MD were established. Pathological changes in cortical neurons were assessed by hematoxylin and eosin (H&E) and thionine staining. The expression of nuclear receptor-related factor 1 (NURR1) and that of the ERS-related proteins glucose-regulated protein 78 (GRP78), p-eIF2α, activating transcription factor 6 (ATF6), and CHOP in cortical neurons was assessed by immunohistochemistry. Double immunofluorescence labeling was used to observe the expression of Ki-67.

RESULTS

H&E and thionine staining revealed that AME resulted in pyknotic changes in cortical neurons. With prolonged morphine exposure, the number of pyknotic neurons was significantly increased, the protein expression of Ki-67 and NURR1 was significantly decreased, and the protein levels of GRP78, p-eIF2α, ATF6, and CHOP showed marked dynamic changes.

CONCLUSION

AME and different durations of MD caused varying degrees of pathological changes in the cortex. Furthermore, the dynamic changes observed in ERS-related protein expression suggested that ERS may be associated with cortical injury. Different durations of MD inhibited the proliferation, differentiation, and migration of newborn neurons, which may affect the nerve repair process after injury.

摘要

目的

本研究旨在观察急性吗啡暴露（AME）及不同时长吗啡依赖（MD）大鼠大脑皮质的病理损伤，探讨内质网应激（ERS）是否参与损伤过程，并评估吗啡暴露对新生神经元增殖和分化的影响。

方法

建立AME及不同时长MD的大鼠模型。通过苏木精-伊红（H&E）染色和硫堇染色评估皮质神经元的病理变化。采用免疫组织化学法评估皮质神经元中核受体相关因子1（NURR1）以及ERS相关蛋白葡萄糖调节蛋白78（GRP78）、磷酸化真核翻译起始因子2α（p-eIF2α）、活化转录因子6（ATF6）和C/EBP同源蛋白（CHOP）的表达。运用双重免疫荧光标记观察Ki-67的表达。

结果

H&E染色和硫堇染色显示，AME导致皮质神经元出现核固缩变化。随着吗啡暴露时间延长，核固缩神经元数量显著增加，Ki-67和NURR1的蛋白表达显著降低，GRP78、p-eIF2α、ATF6和CHOP的蛋白水平呈现明显的动态变化。

结论

AME及不同时长的MD导致皮质出现不同程度的病理变化。此外，ERS相关蛋白表达的动态变化表明ERS可能与皮质损伤有关。不同时长的MD抑制了新生神经元的增殖、分化和迁移，这可能会影响损伤后的神经修复过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/84128000a223/fnins-15-618190-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/112bc4ab05b3/fnins-15-618190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/6630aabf6141/fnins-15-618190-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/5bdcd2691754/fnins-15-618190-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/d5151ffe33ce/fnins-15-618190-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/cd480d7cc852/fnins-15-618190-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/c6dd1fb67c47/fnins-15-618190-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/b4a8ec1b17fa/fnins-15-618190-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/1897859f35de/fnins-15-618190-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/84128000a223/fnins-15-618190-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/112bc4ab05b3/fnins-15-618190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/6630aabf6141/fnins-15-618190-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/5bdcd2691754/fnins-15-618190-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/d5151ffe33ce/fnins-15-618190-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/cd480d7cc852/fnins-15-618190-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/c6dd1fb67c47/fnins-15-618190-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/b4a8ec1b17fa/fnins-15-618190-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/1897859f35de/fnins-15-618190-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/177a/7935558/84128000a223/fnins-15-618190-g009.jpg

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